CBF changes and cerebral energy metabolism during hypervolemia, hemodilution, and hypertension therapy in patients with poor-grade subarachnoid hemorrhage

OBJECTIVEDespite the multifactorial pathogenesis of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH), augmentation of cerebral blood flow (CBF) is still considered essential in the clinical management of DCI. The aim of this prospective observational study was to investigate cerebral metabolic changes in relation to CBF during therapeutic hypervolemia, hemodilution, and hypertension (HHH) therapy in poor-grade SAH patients with DCI.METHODSCBF was assessed by bedside xenon-enhanced CT at days 0–3, 4–7, and 8–12, and the cerebral metabolic state by cerebral microdialysis (CMD), analyzing glucose, lactate, pyruvate, and glutamate hourly. At clinical suspicion of DCI, HHH therapy was instituted for 5 days. CBF measurements and CMD data at baseline and during HHH therapy were required for study inclusion. Non-DCI patients with measurements in corresponding time windows were included as a reference group.RESULTSIn DCI patients receiving HHH therapy (n = 12), global cortical CBF increased from 30.4 ml/100 g/min (IQR 25.1–33.8 ml/100 g/min) to 38.4 ml/100 g/min (IQR 34.2–46.1 ml/100 g/min; p = 0.006). The energy metabolic CMD parameters stayed statistically unchanged with a lactate/pyruvate (L/P) ratio of 26.9 (IQR 22.9–48.5) at baseline and 31.6 (IQR 22.4–35.7) during HHH. Categorized by energy metabolic patterns during HHH, no patient had severe ischemia, 8 showed derangement corresponding to mitochondrial dysfunction, and 4 were normal. The reference group of non-DCI patients (n = 11) had higher CBF and lower L/P ratios at baseline with no change over time, and the metabolic pattern was normal in all these patients.CONCLUSIONSGlobal and regional CBF improved and the cerebral energy metabolic CMD parameters stayed statistically unchanged during HHH therapy in DCI patients. None of the patients developed metabolic signs of severe ischemia, but a disturbed energy metabolic pattern was a common occurrence, possibly explained by mitochondrial dysfunction despite improved microcirculation.

Cerebral Vasospasm in Subarachnoid Haemorrhage

In the second and third weeks after a subarachnoid haemorrhage a series of mechanisms causes a decrease of the diameter of the cerebral vessels. These phenomena are globally included in the term “vasospasm”. A certain degree of vasospasm is found in the majority of the patients after a subarachnoid bleeding. This can be detected by instrumental examinations, in particular trans-cranial doppler and angiography. However, only a minor percentage of these patients will suffer clinical consequences. The vasospasm is currently treated by hypertensive-hypervolemic-haemodilution therapy (the so called “HHH” therapy), or may be treated by selective injection of vasoactive substances (Papaverine, nimodipine) or by mechanical dilatation of the involved vessels with balloons, mainly because of an improved medical management and a better monitoring of critical patients the incidence of clinical vasospasm has decreased in the recent years.